The purpose of the Infrastructure and Opportunity Fund IVIanagement (lOFM) Core is to create and facilitate collaborations between NIAID-sponsored AADCRCs through new clinical researcii and resource development projects;support promising opportunities that advance an understanding of the pathophysiology of asthma and allergic diseases;and develop improved therapies to reduce or prevent disease progression. Since the focus of the SA-AADCRC emphasizes the Induction and exacerbation of Inflammatory pathways and tissue Injury, as viewed from the perspective of Mycoplasma pneumoniae and its unique ADP ribosylating and vacuolating toxin, designated Community Acquired Respiratory Distress Syndrome Toxin (CARDS TX), many collaborative and synergetic opportunities exist among AADCRC members. The ability of CARDS TX alone to both Induce asthma-like disease and exacerbate allergic Inflammation places this remarkable pathogenic factor as a potential sole mediator, or amplifier, or co-factor in a broad range of ainA/ay conditions that lead to acute and chronic pulmonary pathologies. Therefore, the relationships between M. pneumoniae and other environmental triggers could be very Impactful and revealing, as M. pneumoniae infections are common and persistent and CARDS TX produces lymphocytic Inflammation, mucous hypersecretion, and hyperreactivity. Importantly, CARDS TX protein can be readily detected in airway secretions of asthmatic subjects and by Itself exacerbates eosinophilic/lymphocytic Inflammation and hyperresponsiveness to ovalbumin and house dust mite In the murine model. Collaborations with AADCRCs that examine viral and other Infectious pollutants and allergens could lead to understanding how certain individuals manifest exaggerated Inflammatory responsiveness as a result of M. pneumoniae and CARDS TX presence/persistence. Also, recombinant CARDS TX and other related reagents could serve as useful tools to share among AADCRCs for studying the molecular and pathophysiological mechanisms that precipitate asthma-like pulmonary Inflammation and associated pathologies.

Public Health Relevance

The Infrastructure and Opportunity Fund Management Core could provide important opportunities for collaborations between the San Antonio AADCRC and other Centers, as Mycoplasma pneumoniae and its ADP ribosylating and vacuolating toxin (CARDS TX) induce and exacerbate allergic inflammation. Therefore, lOFM Core-supported collaborations that link the SA-AADCRC with other Centers studying inflammatory triggers of asthma and allergic diseases could lead to innovative therapies and improved diagnostic assessments of patient wellness and prognosis.

National Institute of Health (NIH)
Research Program--Cooperative Agreements (U19)
Project #
Application #
Study Section
Special Emphasis Panel (ZAI1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Texas Health Science Center
San Antonio
United States
Zip Code
Ji, Hong; Zhang, Xue; Oh, Sunghee et al. (2015) Dynamic transcriptional and epigenomic reprogramming from pediatric nasal epithelial cells to induced pluripotent stem cells. J Allergy Clin Immunol 135:236-44
Medina, Jorge L; Coalson, Jacqueline J; Brooks, Edward G et al. (2014) Mycoplasma pneumoniae CARDS toxin exacerbates ovalbumin-induced asthma-like inflammation in BALB/c mice. PLoS One 9:e102613
Kannan, Thirumalai R; Krishnan, Manickam; Ramasamy, Kumaraguruparan et al. (2014) Functional mapping of community-acquired respiratory distress syndrome (CARDS) toxin of Mycoplasma pneumoniae defines regions with ADP-ribosyltransferase, vacuolating and receptor-binding activities. Mol Microbiol 93:568-81
Somarajan, Sudha R; Al-Asadi, Fadi; Ramasamy, Kumaraguruparan et al. (2014) Annexin A2 mediates Mycoplasma pneumoniae community-acquired respiratory distress syndrome toxin binding to eukaryotic cells. MBio 5:
Burks, Margaret L; Brooks, Edward G; Hill, Vanessa L et al. (2013) Assessing proxy reports: agreement between children with asthma and their caregivers on quality of life. Ann Allergy Asthma Immunol 111:14-9
Krishnan, Manickam; Kannan, T R; Baseman, Joel B (2013) Mycoplasma pneumoniae CARDS toxin is internalized via clathrin-mediated endocytosis. PLoS One 8:e62706
Kannan, T R; Hardy, R D; Coalson, J J et al. (2012) Fatal outcomes in family transmission of Mycoplasma pneumoniae. Clin Infect Dis 54:225-31
Medina, Jorge L; Coalson, Jacqueline J; Brooks, Edward G et al. (2012) Mycoplasma pneumoniae CARDS toxin induces pulmonary eosinophilic and lymphocytic inflammation. Am J Respir Cell Mol Biol 46:815-22
Johnson, Coreen; Kannan, T R; Baseman, Joel B (2011) Cellular vacuoles induced by Mycoplasma pneumoniae CARDS toxin originate from Rab9-associated compartments. PLoS One 6:e22877
Muir, Mark T; Cohn, Stephen M; Louden, Christopher et al. (2011) Novel toxin assays implicate Mycoplasma pneumoniae in prolonged ventilator course and hypoxemia. Chest 139:305-10

Showing the most recent 10 out of 20 publications